A variety of halogenated hydrocarbons are used by man for such diverse things as anesthetics and insecticides. A proportion of these agents produce liver injury both acutely and chronically. The hepatotoxicity of CCl4 may represent a model system to study the mechanisms involved in cell injury and in regeneration following injury. Critical analysis of the processes involved may provide clues to devise better screening tests for potential toxicity of new compounds. These studies propose to investigate the mechanism of enzymic dehalogenation and its role in CCl4 injury, and to explore changes in the cellular membranous structures during the development of the injury. Specifically structural and functional changes in the plasmalemma will be detailed. The hypothesis that plasmalemma changes are a key change to cell death will be tested. The role of altered translocation in decreased protein synthesis will be sought. A comparison of these changes with halothane induced injury will also be made.